Novel Combination of Lateral Interbody Fusion and Endoscopic Ipsi-Contra Decompression for Severe Stenosis From Lumbar Spondylolisthesis: A Case Report.

Minimally invasive surgical approaches to the spine that leverage indirect decompression are gaining increasing popularity. While there is excellent literature on the value of indirect decompression, there are limitations to this procedure. Specifically, in patients with severe stenosis and neurogenic claudication, there is a concern among many surgeons regarding the adequacy of indirect decompression alone. In these cases, the lateral approach is often abandoned in favor of an open posterior or posterior minimally invasive approach. Unfortunately, some of the distinct benefits of the direct lateral approach are then lost. Here, we present the case of a 58-year-old male who underwent an L4-L5 lateral interbody fusion with an endoscopic ipsi-contra decompression to achieve both direct and indirect treatment of severe neuroforaminal and central stenosis. From this strategy, this patient had complete pre-operative symptom resolution and was able to return to work immediately after surgery without significant restriction. Combining the benefits of direct and indirect using an ultra-minimally invasive decompressive approach offers a potential solution.

Surgical Management of Thoracolumbar Adjacent Segment Disease: Techniques and Outcomes in 107 Patients Undergoing Surgical Intervention.

BACKGROUND: Adjacent segment disease (ASD) is a known sequela of thoracolumbar instrumented fusions. Various surgical options are available to address ASD in patients with intractable symptoms who have failed conservative measures. However, the optimal treatment strategy for symptomatic ASD has not been established. We examined several clinical outcomes utilizing different surgical interventions for symptomatic ASD. METHODS: A retrospective review was performed for a consecutive series of patients undergoing revision surgery for thoracolumbar ASD between October 2011 and February 2022. Patients were treated with endoscopic decompression (N = 17), microdiscectomy (N = 9), lateral lumbar interbody fusion (LLIF; N = 26), or open laminectomy and fusion (LF; N = 55). The primary outcomes compared between groups were re-operation rates and numeric pain scores for leg and back at 2 weeks, 10 weeks, 6 months, and 12 months postoperation. Secondary outcomes included time to re-operation, estimated blood loss, and length of stay. RESULTS: Of the 257 patients who underwent revision surgery for symptomatic ASD, 107 patients met inclusion criteria with a minimum of 1-year follow-up. The mean age of all patients was 67.90 ± 10.51 years. There was no statistically significant difference between groups in age, gender, preoperative American Society of Anesthesiologists scoring, number of previously fused levels, or preoperative numeric leg and back pain scores. The re-operation rates were significantly lower in LF (12.7%) and LLIF cohorts (19.2%) compared with microdiscectomy (33%) and endoscopic decompression (52.9%; P = 0.005). Only LF and LLIF cohorts experienced significantly decreased pain scores at all 4 follow-up visits (2 weeks, 10 weeks, 6 months, and 12 months; P < 0.001 and P < 0.05, respectively) relative to preoperative scores. CONCLUSION: Symptomatic ASD often requires treatment with revision surgery. Fusion surgeries (either stand-alone lateral interbody or posterolateral with instrumentation) were most effective and durable with respect to alleviating pain and avoiding additional revisions within the first 12 months following revision surgery. CLINICAL RELEVANCE: This study emphasizes the importance of risk-stratifying patients to identify the least invasive approach that treats their symptoms and reduces the risk of future surgeries.

Pericyte infection by HIV-1: a fatal attraction.

While HIV-1 is primarily an infection of CD4 + T cells, there is an emerging interest towards understanding how infection of other cell types can contribute to HIV-associated comorbidities. For HIV-1 to cross from the blood stream into tissues, the virus must come in direct contact with the vascular endothelium, including pericytes that envelope vascular endothelial cells. Pericytes are multifunctional cells that have been recognized for their essential role in angiogenesis, vessel maintenance, and blood flow rate. Most importantly, recent evidence has shown that pericytes can be a target of HIV-1 infection and support an active stage of the viral life cycle, with latency also suggested by in vitro data. Pericyte infection by HIV-1 has been confirmed in the postmortem human brains and in lungs from SIV-infected macaques. Moreover, pericyte dysfunction has been implicated in a variety of pathologies ranging from ischemic stroke to diabetes, which are common comorbidities among people with HIV-1. In this review, we discuss the role of pericytes during HIV-1 infection and their contribution to the progression of HIV-associated comorbidities.

Brain endothelium-derived extracellular vesicles containing amyloid-beta induce mitochondrial alterations in neural progenitor cells.

Aim: Elevated brain deposits of amyloid beta (Aß40) contribute to neuropathology and cognitive dysfunction in Alzheimer's disease (AD). However, the role of the blood-brain barrier (BBB) as an interface for the transfer of Aß40 from the periphery into the brain is not well characterized. In addition, a substantial population of neural progenitor cells (NPCs) resides in close proximity to brain capillaries that form the BBB. The aim of this study is to understand the impact of brain endothelium-derived extracellular vesicles (EV) containing Aß40 on metabolic functions and differentiation of NPCs. Methods: Endothelial EVs were derived from an in vitro model of the brain endothelium treated with 100 nM Aß40 or PBS. We then analyzed the impact of these EVs on mitochondrial morphology and bioenergetic disruption of NPCs. In addition, NPCs were differentiated and neurite development upon exposure to EVs was assessed using the IncuCyte Zoom live cell imaging system. Results: We demonstrate that physiological concentrations of Aß40 can be transferred to accumulate in NPCs via endothelial EVs. This transfer results in mitochondrial dysfunction, disrupting crista morphology, metabolic rates, fusion and fission dynamics of NPCs, as well as their neurite development. Conclusion: Intercellular transfer of Aß40 is carried out by brain endothelium-derived EVs, which can affect NPC differentiation and induce mitochondrial dysfunction, leading to aberrant neurogenesis. This has pathological implications because NPCs growing into neurons are incorporated into cerebral structures involved in learning and memory, two common phenotypes affected in AD and related dementias.